Vestibular stimulator

ABSTRACT

A method for providing relief from Meniere&#39;s disease, includes reversibly disabling vestibular function following detection of an attack of Meniere&#39;s disease following detection of an attack of Meniere&#39;s disease.

RELATED APPLICATION

This application is a divisional of pending U.S. application Ser. No.10/738,920, filed Dec. 16, 2003, which claims the benefit of thepriority date of U.S. provisional application 60/433,946, filed Dec. 17,2002 the contents of which are incorporated herein by reference.

FIELD OF INVENTION

This invention relates to treatment for vestibular dysfunction.

BACKGROUND

When a normal person is stationary, the neurons associated with thevestibular system carry pulse trains that, on average, have a nearlyconstant pulse-repetition frequency. If the patient changes spatialorientation, the average pulse-repetition frequency of the pulse trainschanges. These pulse trains, hereafter referred to as the “vestibularsignal”, are transmitted to the brain via the vestibular nerve. On thebasis of changes in the average pulse-repetition frequency, the braindetermines the patient's spatial orientation and motion.

The vestibular system is not the brain's only source of informationconcerning the patient's spatial orientation. Both the vision and othersensory systems, such as the proprioceptive and tactile systems, provideadditional cues. The brain reconciles these additional cues withinformation from the vestibular system. To the extent that these cuesare inconsistent with each other, the patient experiences dizziness.

In one afflicted with Meniere's disease, the vestibular system, for noapparent reason, suddenly begins varying the pulse-repetition frequencyof the vestibular signal even when the patient is stationary. Thisresults in severe dizziness. Then, and again for no apparent reason, thevestibular system begins generating a vestibular signal consistent withthe person's spatial orientation, thereby ending the person's symptoms.

Known treatments for Meniere's disease include surgical removal of thepatient's vestibule. Another treatment involves perfusion of ototoxicdrugs that permanently destroy the cilia within the vestibule. As aresult, these treatments result in the permanent loss of the patient'ssense of balance.

Less draconian treatments for Meniere's disease include the introductionof drugs having questionable efficacy, acupuncture, and varioushomeopathic remedies. These treatments have not shown consistentsuccess.

SUMMARY

In one aspect, the invention includes an apparatus for stimulating thevestibular system. The apparatus includes an actuator disposed tointeract with the vestibular nerve and a controller for causing theactuator to interact with the vestibular nerve. The result of theinteraction is that the brain receives a stationary signal.

Embodiments of the invention include those in which the actuator has animplantable electrode, an antenna, an external electrode, an implantableelectrode having a receiver for communication with a transmitter outsidethe patient, or a magnetic field source, each of which is incommunication with the vestibular nerve. Other embodiments include thosein which a vibrating element is adapted to mechanically stimulate thevestibule.

Other embodiments of the invention include those in which the actuatorincludes a chemical delivery system adapted for delivering a chemicalagent to an active region. Once in the active region, the chemical agentinteracts with the vestibular nerve. Such a chemical delivery systemmight include, for example, a reservoir for containing the chemicalagent, and a pump for delivering the chemical agent from the reservoirto the active region.

Some embodiments of the apparatus include an externally actuated switchin communication with the controller for enabling external control of aninteraction with the vestibular nerve. In other embodiments, theapparatus includes a sensor adapted to detect a first signal on thevestibular nerve. Such a sensor is in communication with the controllerfor causing the controller to generate a second signal in response tothe first signal.

In some embodiments, the controller is configured to cause the actuatorto generate a signal that, when combined with a non-stationary signalpresent on the vestibular nerve, causes a stationary signal to betransmitted to the brain.

Another aspect of the invention is a method for providing relief fromMeniere's disease by reversibly disabling vestibular function followingdetection of an attack of Meniere's disease.

In certain practices of the invention, reversibly disabling vestibularfunction includes temporarily causing the vestibular nerve to carry astationary signal to the brain. This can be achieved, for example, bycausing the vestibular nerve to carry a jamming signal that, whencombined with a non-stationary signal present on the vestibular nerve,causes the vestibular nerve to carry a stationary signal to the brain.One example of a jamming signal is a pulse train having a selected pulserepetition frequency.

The jamming signal can be generated in a variety of ways, for example byelectrical or electromagnetic stimulation of the vestibular nerve, bymechanically stimulating the vestibule, or by exposing the vestibularnerve to a chemical agent.

In one practice of the invention, the chemical agent is aneurotransmitter. However, the chemical agent can also be anerve-impulse blocking agent.

In another practice of the invention, the method includes detectingonset of an attack of Meniere's disease, and applying a jamming signalfollowing detection of an attack. Other practices of the inventioninclude those in which the jamming signal is removed at the end of anattack of Meniere's disease.

Meniere's disease is episodic in nature. During an attack, the patientexperiences severe discomfort. However, between attacks, the patient islargely asymptomatic. Conventional methods of treating Meniere's diseasedisable vestibular function permanently, thereby leaving the patientwith no vestibular function even during asymptomatic periods. Theinvention provides relief from the disease by disabling vestibularfunction only during the attack itself, but not during the periodbetween such attacks. As a result, the patient's vestibular function isavailable during asymptomatic periods.

Another aspect of the invention is a method for providing relief fromhemineglect by isothermally stimulating vestibular function.

In certain practices of the invention, stimulating vestibular functionincludes causing the vestibular nerve to carry a stationary signal tothe brain. This can be achieved, for example, by causing the vestibularnerve to carry a jamming signal that, when combined with anon-stationary signal present on the vestibular nerve, causes thevestibular nerve to carry a stationary signal to the brain. One exampleof a jamming signal is a pulse train having a selected pulse repetitionfrequency.

The jamming signal can be generated in a variety of ways, for example byelectrical stimulation of the vestibular nerve, by mechanicallystimulating the vestibule, or by exposing the vestibular nerve to achemical agent.

In one practice of the invention, the chemical agent is aneurotransmitter. However, the chemical agent can also be anerve-impulse blocking agent.

These and other features and advantages of the invention will beapparent from the following detailed description and the accompanyingfigures, in which:

BRIEF DESCRIPTION OF THE DRAWINGS

FIG. 1 is an apparatus according to the invention;

FIG. 2 is an embodiment in which the actuator of FIG. 1 is an electrode;

FIG. 3 is a wireless embodiment of the apparatus of FIG. 2;

FIG. 4 is an embodiment in which the actuator of FIG. 1 is an antenna;

FIG. 5 is an embodiment having an automatic control unit with a feedbackloop;

FIG. 6 is an embodiment in which the actuator of FIG. 1 is a coil forgenerating a magnetic field;

FIG. 7 is an embodiment having an actuator that shakes the vestibule;and

FIG. 8 is an embodiment in which an actuator applies chemical agents tothe vestibular nerve area.

DETAILED DESRCIPTION

FIG. 1 shows an apparatus 10 for providing symptomatic relief fromMeniere's disease. The apparatus includes an actuator 12 incommunication with the vestibular nerve 14. A control unit 16 inelectrical communication with the actuator 12 provides control over ajamming signal present at the actuator 12. As used herein, electricalcommunication encompasses both a wireless connection, in whichcommunication is carried out by electromagnetic waves, and a wiredconnection. In one particular embodiment disclosed herein, this jammingsignal is a pulse train having a controllable pulse amplitude andpulse-repetition frequency, both of which are set by the control unit16. However, the jamming signal can also be any other time-varyingstimulus. Examples of other jamming signals include sinusoidal signalsor any other oscillatory signals.

A power source 18, such as a rechargeable battery, provides power toboth the actuator 12 and the control unit 16.

During an attack of Meniere's disease, a vestibular signal on thevestibular nerve develops time-varying changes in the neuralpulse-repetition frequency even when the patient's spatial orientationis not changing. A time-varying signal of this type, in which theamplitude or frequency is modulated with time, is often referred to as a“non-stationary” signal.

The patient interprets a non-stationary signal on the vestibular nerveas indicating a change in his spatial orientation, even when his spatialorientation has not changed at all. The vestibular signal, together withthe mismatch between the vestibular signal and other motion cuesavailable to the brain results in dizziness and discomfort.

The apparatus 10 relieves the discomfort of Meniere's disease bytemporarily and reversibly disabling vestibular function. It does so byjamming the vestibular signal with the jamming signal. Thecharacteristics of this are selected so that the combination of thejamming signal and the vestibular signal results in a signal having aconstant pulse-repetition frequency. Examples of characteristics thatcan be selected to achieve this are the jamming signal's pulse amplitudeand pulse-repetition frequency.

Proper selection of the jamming signal's characteristics causes thebrain to receive a stationary signal instead of the non-stationarysignal that characterizes Meniere's disease. To the extent that thepatient remains stationary during the attack, the brain receives asignal consistent with the patient's constant spatial orientation. Sincethe brain now receives a signal consistent with other motion cues, thediscomfort associated with Meniere's disease is alleviated.

The amplitude of the jamming signal depends in part on the type ofactuator 12. In one embodiment, shown in FIG. 2, the actuator 12includes a jamming electrode 20 that is implanted proximate to thevestibular nerve 14. In this case, the amplitude is selected such that acurrent on the order of a milliamp or less is present at the jammingelectrode 20. Communication between the control unit 16 and the jammingelectrode 20 can be established by a wire that perforates the skull.However, to avoid the need to perforate the skull, communication betweenthe control unit 16 and jamming electrode 20 can also be wireless. Thisis achieved by a control unit 16 having a transmitter 21 and an actuator12 having a receiver 23 in communication with the jamming electrode 20,as shown in FIG. [2.5]3.

Another embodiment, shown in FIG. 4, avoids the need to implant byproviding an actuator 12 that includes an antenna or external electrode22 worn by the patient adjacent to the head. In this case, the amplitudeis increased so that the vestibular nerve 14 is illuminated bysufficient power from the actuator 12. Typically, the amplitude israised so that a current on the order of at least tens of milliamps ispresent on the antenna 22.

The jamming signal characteristics are selected such that the resultingcombination of the jamming signal and the vestibular signal results in asignal having a constant pulse-repetition frequency. A time-varyingsignal of this type, the spectrum of which is essentially constant intime, will be referred to herein as a “stationary signal.”In oneembodiment, the pulse-repetition frequency is approximately equal to themaximum neuron firing rate, which is typically on the order of 450 Hz.This pulse-repetition frequency is likely to result in the synchronousfiring of neurons at or near their maximum firing rate. However, it maybe useful in some cases to have a much higher pulse-repetitionfrequency, for example in the 1-10 kilohertz range, so that neurons fireasynchronously.

The jamming signal need only be on during an attack of Meniere'sdisease. When the attack subsides, the jamming signal is removed and thepatient regains normal vestibular function. The control unit 16 thusprovides a mechanism for applying and removing the jamming signal.

In one embodiment, the control unit 16 has a patient-accessible switch24, as shown in FIG. 1. When the patient feels the onset of an attack,he uses the switch to apply the jamming signal. A disadvantage of thistype of control unit 16 is that because the jamming signal masks thesymptoms of the attack, the patient is unable to tell whether the attackis over.

In the embodiment having a patient-accessible switch 24, the patient cansimply use the switch to turn off the jamming signal after a reasonabletime has elapsed. The resulting change in the pulse-repetition frequencyof the signal received by the brain may result in some dizziness.However, if the attack of Meniere's disease is in fact over, thisdizziness should fade shortly. If the dizziness does not fade, thepatient uses the switch 24 to turn the jamming signal on again.

Alternatively, the switch 24 can include a timer that automaticallyturns the jamming signal off after the lapse of a pre-determined jamminginterval. In some embodiments, the length of the jamming interval isuser-controlled, whereas in others, the length of the jamming intervalis hard-wired into the control unit 16. If the dizziness does not fadeafter the stimulation has been turned off, the patient uses the switch24 to turn the jamming signal on again.

The control unit 16 can also be an automatic control unit 16 having afeedback loop, as shown in FIG. 5. In this case, a sensor electrode 26is implanted proximate to the vestibular nerve 14 to measure thevestibular signal. When the control unit 16 detects appropriatetime-varying changes in the pulse-repetition frequency of the vestibularsignal, it causes the control unit 16 to apply the jamming signal to thejamming electrode 20. In this case, the jamming signal characteristicscan be made to vary in response to the characteristics of the measuredvestibular signal.

The jamming signal need not be an electrical signal. For example, in theembodiment of FIG. 6, the jamming signal is generated by a magneticfield generated by a coil 28 located outside the patient.

Another embodiment, shown in FIG. 7, generates a jamming signal bymechanical stimulation of the vestibule 30. In this case, apiezoelectric element 32 is implanted proximate to the vestibule 30. Thecontroller sends a jamming signal to the piezoelectric element 32,thereby causing the piezoelectric element 32 to flex and relax at aparticular frequency. The motion of the piezoelectric element 32 istransmitted to the vestibule 30, thereby causing portions of thevestibule 30 to vibrate at that frequency. The vibration of thevestibule 30 causes the generation of an additional component of thevestibular signal. This additional component combines with the componentresulting from the attack of Meniere's disease. Again, by properselection of the pulse-repetition frequency, the signal received by thebrain on the vestibular nerve 14 will again have a constantpulse-repetition frequency.

FIG. 8 shows an embodiment in which chemical agents interfere with thevestibular signal. In this case, the controller drives a pump 34 thatpumps a chemical agent stored in a reservoir 36. The chemical agent canbe a neurotransmitter to be administered to one or more synapses 38 atdoses sufficient to drive repeated firing of the neurons at or close totheir maximum firing rates. Again, this results in the generation of ajamming signal that interferes with, and effectively masks, thevestibular signal. Alternatively, the reservoir 36 can contain aneurosuppressive agent to be applied to the synapses to prevent thevestibular signal from reaching the brain. In this case, the vestibularsignal that reaches the brain has a constant pulse-repetition frequencyof zero.

The apparatus described herein has therapeutic purposes other thantreatment of Meniere's disease. For example, the apparatus can be usedto isothermally stimulate the vestibular system of a stroke victimafflicted with hemineglect. Such stimulation can provide relief fromsymptoms of hemineglect.

The foregoing embodiments of the apparatus all provide temporary andcontrollably reversible disabling of vestibular function by controllablyjamming the vestibular signal with a jamming signal. Other embodimentsare within the scope of the following claims:

1. A method for providing relief from Meniere's disease, the methodcomprising reversibly disabling vestibular function following detectionof an attack of Meniere's disease.
 2. The method of claim 1, whereinreversibly disabling vestibular function comprises temporarily causingthe vestibular nerve to carry a stationary signal to the brain.
 3. Themethod of claim 2, wherein causing the vestibular nerve to carry astationary signal comprises causing the vestibular nerve to carry ajamming signal that, when combined with a non-stationary signal presenton the vestibular nerve, causes the vestibular nerve to carry astationary signal to the brain.
 4. The method of claim 3, whereincausing the vestibular nerve to carry a jamming signal comprisesexposing the vestibular nerve to a pulse train having a selected pulserepetition frequency.
 5. The method of claim 4, further comprisingselecting the pulse repetition frequency to be higher than the maximumpulse repetition frequency of a neuron.
 6. The method of claim 3,wherein causing the vestibular nerve to carry a stationary signalcomprises exposing the vestibular nerve to the jamming signal.
 7. Themethod of claim 3, wherein causing the vestibular nerve to carry astationary signal comprises mechanically stimulating the vestibule tocause a jamming signal on the vestibular nerve.
 8. The method of claim3, wherein causing the vestibular nerve to carry a stationary signalcomprises exposing the vestibular nerve to a chemical agent.
 9. Themethod of claim 8, wherein exposing the vestibular nerve to a chemicalagent comprises exposing the vestibular nerve to a neurotransmitter. 10.The method of claim 8, wherein exposing the vestibular nerve to achemical agent comprises exposing the vestibular nerve to anerve-impulse blocking agent.
 11. The method of claim 2, furthercomprising detecting onset of an attack of Meniere's disease, andapplying a jamming signal following detection of the attack of Meniere'sdisease.
 12. The method of claim 11, further comprising removing thejamming signal following completion of the attack of Meniere's disease.